Secondary Logo

Journal Logo

Original Article

Decreasing Incidences of Gonorrhea- and Chlamydia-Associated Acute Pelvic Inflammatory Disease

A 25-Year Study From an Urban Area of Central Sweden

KAMWENDO, FRANCIS MD*; FORSLIN, LARS MD, PhD*; BODIN, LENNART PhD; DANIELSSON, DAN MD, PhD

Author Information
  • Free

Abstract

ACUTE PELVIC INFLAMMATORY DISEASE (PID) is a serious clinical condition that almost exclusively affects sexually active women in their fertile years. It generally is defined as the acute clinical syndrome of an upper genital tract infection with inflammation, mostly caused by an ascending spread of microorganisms from the vagina or cervix to the endometrium, fallopian tubes, and adjacent structures. Therefore, PID may include endometritis, parametritis, salpingitis, pelvic peritonitis, and pelvic abscess, and occasionally it may involve the appendix (periappendicitis) and the liver capsule (perihepatitis).1–3 Pelvic inflammatory disease and acute salpingitis are diagnoses often used synonymously for ascending infection involving fallopian tubes.3 Recurrences are common. Infertility, chronic lower abdominal pain, and increased risk for ectopic pregnancy are welldocumented sequelae.1–3 The patient suffers psychological stress and loss of productivity, and the costs to the society are considerable.4–7

Sexually transmitted diseases (STD) agents and/or microorganisms of the endogenous flora of the lower genital tract are the two major groups of organisms associated with an ascending infection in acute PID.3 Of the latter group, facultative and obligate anaerobic grampositive and gram-negative bacteria, as well as Mycoplasma and Ureaplasma, have been implicated with no particular preference for one or another. Infections with organisms of this group usually are polymicrobial.3 Among STD agents, Neisseria gonorrhoeae has long8 been considered a major etiological agent in PID, with the terms gonococcal versus nongonococcal PID or salpingitis as accepted terminologies3,9 It has been reported that PID develops in 10% to 15% of women with gonorrhea and that 40% or more of women admitted to the hospital because of PID had gonorrhea.2,10–13

In addition to the gonococcus, Chlamydia trachomatis has proved to be a significant bacterial STD agent. In the mid-1970s, such infections were documented as an important etiology of PID.3,14–17 Pelvic inflammatory disease is one of the extrapulmonary manifestations of Mycobacterium tuberculosis infection,18 but this is a rare complication in Scandinavia.19 Although Herpes simplex virus,20 cytomegalovirus,21 and human immunodeficiency viruses22 have been isolated from some patients with PID, the role of viruses as causative agents for PID is yet to be established.23

Though the endogenous microbial flora of the genital tract may play a role in the development of acute PID, it seems reasonable to postulate that the proportion of females falling ill with this condition will be reflected by the overall incidence of gonorrhea and genital C. trachomatis infections in the community. When urogenital gonorrhea started to decrease in Sweden in the early 1970s, we showed that the relative incidence of gonococcal salpingitis decreased even more.9 These observations were confirmed in a study from the early 1980s.13 At the same time, however, there were more patients with nongonococcal salpingitis. Part of this increase might have been caused by a high incidence of genital C. trachomatis infections, documented in the late 1970s and early 1980s.16,17 In Sweden, gonorrhea has been a reportable contagious disease since 1919. Genital C. trachomatis infection was included in this legislation in April 1988 and was aimed at reducing and perhaps controlling these infections. According to this legislation, both the patient and the doctor have responsibilities with regard to diagnosis, treatment, follow-up, and contact tracing.24 Since 1984, we have subjected male partners of our patients with acute PID to antibiotic treatment because we have found that at least 60% of those males had either specific or nonspecific urethritis.25 The question then arises whether related measures influence the total and relative incidences of acute PID and the rate of recurrence of this condition. These matters will be elucidated in this article, a retrospective investigation of acute PID during a 25-year-period (1970 to 1994) in the district of Örebro, an urban area of central Sweden.

Materials and Methods

Patients and Diagnostic Criteria

The study covers a period of 25 years, from January 1, 1970 to December 31, 1994, and includes 2499 admissions for acute PID at the Department of Gynaecology, Örebro Medical Centre Hospital, Örebro, Sweden. Patients' charts were traced using the hospital's register, which is compiled according to the World Health Organization's international nomenclature and numbering of diagnoses. The county's central registry for hospital diagnoses since 1974 was used as a control to check whether our retrieval of charts was correct.

The same clinical procedures were followed during the study period; thus, all patients attending the hospital with a clinically overt or suspected acute PID routinely were admitted. This was checked continuously by two of the authors (LF, DD), senior physicians for the entire study period. Diagnosis was based on the following criteria: history of pain in the lower abdomen, with palpable adnexal mass or motion tenderness, and objective signs of lower genital tract infection (pus from cervical ostium, wet smear showing on microscopy at ×400 more polymorphonuclear leukocytes than epithelial cells,26 or both), in addition to either fever (temperature ≥ 38°C), menstrual irregularity, elevated erythrocyte sedimentation rate >15 mm/hour, or dysuria. Physical examination was repeated, and the clinical signs and symptoms were judged by a senior physician the morning after admission. Involvement of the fallopian tubes was visualized by laparoscopy (or laparotomy) using the criteria described by Jacobson and Weström27 in approximately 60% to 65% of the 2499 patients who fulfilled the clinical criteria for PID. The group with laparoscopically verified PID had proportionally fewer patients with gonorrhea and/or genital C. trachomatis infection when we compared the early 1970s with the early 1980s.13

Recurrence

Recurrence is defined as the reappearance of the typical signs and symptoms of acute PID in a person previously considered clinically cured of the disease. Recurrence rate is the percentage of patients with recurrences over the total number of patients with acute PID during a given period of time.

Bacteriology

On the day the patient was admitted to the hospital or the next morning when the patient was reexamined, specimens for gonococci culture were taken from the patient's urethra, cervical os, and, occasionally, the rectal mucosa with a charcoal-treated cotton swab and were transported to the laboratory in modified Stuart's transport medium without delay. At the laboratory, the specimens were cultured on selective and nonselective gonococcal media for the detection and identification of N. gonorrhoeae as described elsewhere.28 Complete data were available for the 2499 patients.

Routine diagnosis for genital C. trachomatis infection of our patients started June 1, 1980. Specimens for C. trachomatis were collected from the urethra and cervical os using a cotton-tipped aluminum wire (ENT; Medical Wire and Equipment, Corsham, UK) and were taken before those for gonococcal culture. Transport of specimens and culture and identification of inclusion bodies were performed as described elsewhere.29 As an alternative to culture, enzyme immunoassays for the detection of C. trachomatis antigens were used.29 Complete data were available for 1030 patients for the period 1981 to 1994.

Statistics

Incidence was calculated using official population statistics for the catchment area of the hospital to represent the average population in 5-year age groups and 5-year periods. For the oldest age group (women 35 years and older), the incidence was calculated for the 35- to 54-year range, and for the youngest group (≤14 years), the calculation was based on the 10- to 14-year range. All numbers represent total enumerations within the catchment area during the studied time period.

Results

Admissions for Acute Pelvic Inflammatory Disease, 1970 to 1994

Figure 1 shows that the yearly number of patients admitted and treated for acute PID differed only slightly in the early 1970s (1970 to 1973) and the early and middle 1980s (1980 to 1986) from year to year. The differences were ≤15%, with the exception of a decrease of 16.1% (20 of 124; from 124 to 104) for 1971 to 1972. This was in contrast to the large increase, 73% (76 of 104; from 104 to 180) for 1973 to 1976 and the relatively large fluctuations in the middle and late 1970s. From 1987, there has been a steady decrease in admissions for acute PID; the lowest figures for the entire study period have been noted in the last 8 years, from 1987 to 1994.

Fig. 1
Fig. 1:
The yearly number of patients admitted and treated for acute pelvic inflammatory disease (PID) and the percentage rates for those with concomitant genital Neisseria gonorrheae (N.g.) or Chlamydia trachomatis (C.t.) infection during a 25-year-period from 1970 to 1994. Complete data for C. trachomatis in our hospital are from January 1, 1981.

Age Distribution and Incidence Rates

The number of patients with acute PID and their relative age distribution within the 5-year ranges (≤14 years, 15 to 19 years, and so on) for each of the 5-year calendar periods are shown in Table 1. Correspondingly, the incidence rates per 1000 women (related to the age groups in the catchment area; see Materials and Methods) are shown in Figure 2.

TABLE 1
TABLE 1:
Patients With Acute Pelvic Inflammatory Disease Within Different Age Groups During the Study Period 1970–1994*
Fig. 2
Fig. 2:
The incidence rates of acute pelvic inflammatory disease per 1000 women in the catchment area for Örebro Medical Centre Hospital, Örebro, Sweden. The patients were divided into six age groups, and incidences were calculated per 5-year-period during the study period from 1970 to 1994.

As can be seen, the incidence rates in the 5-year groups differed during the studied 25-year period, as did the relative age distribution. In 1970 to 1974, the 15- to 19-year-old group constituted 28.9% of the patients, but in 1990 to 1994, it constituted only 12.9%. For the oldest age group, the development was the opposite: from 9.1% in 1970 to 1974 to 24.9% in 1990 to 1994. In fact, this was the second largest group in that last 5-year period (Table 1). However, the incidence rate was relatively stable for this age group during the five studied 5-year periods (Fig. 2). This was also true for the youngest age group (≤14 years) in which few patients were admitted, especially during the last 10 years. In contrast, the total number of patients and the incidence rates in the 15- to 34-year-old group varied considerably. They accounted for the large increase in the middle and late 1970s. This was especially true of the 20- to 24-year-old group. Of note is the fact that the 15- to 19-year-old group had the highest incidence rate in 1970 to 1974, although the relative age distribution was 2.6% less than for those 20 to 24 years of age (Table 1, Figure 2). From 1980, the incidence rates have decreased greatly for the 15- to 34-year-old groups and was more pronounced for the 15- to 19-year-old group for the last 5-year period.

Gonococcal- and Chlamydial-Associated Pelvic Inflammatory Disease

As can be seen from Figure 1 and Table 2 the decrease in admissions for acute PID during the last 10 years coincided with the nearly complete disappearance of gonococcal-associated and the decrease of chlamydial-associated acute PID. The changes were obvious for all age groups but were most pronounced in the 15- to 19-, 20- to 24-, and 25- to 29-year-old groups (Table 2). Gonorrhea and chlamydial infection were common among those age groups in 1980 to 1984, and 15% to 20% of the patients had both N. gonorrhoeae and C. trachomatis infection (not shown in Table 2). There are reasons to believe those figures were higher still in 1970 to 1974 and in 1975 to 1979.12 In the last 5-year period, gonorrhea did not occur in any age group, whereas chlamydial infections still occurred in 21.4% and 17.4% of those 15 to 19 and 20 to 24 years of age and in 2.6% and 3.8% of those 25 to 29 and 30 to 34 years of age. No chlamydial infections were found in women 35 years or older and in girls 14 years or younger.

TABLE 2
TABLE 2:
Acute Pelvic Inflammatory Disease and Concomitant Gonorrhea or Genital Chlamydial Infection

Pelvic Inflammatory Disease Recurrence Rates

Pelvic inflammatory disease recurrence rates decreased during the studied 25-year-period. For example, in the 1975 to 1978 cohort of 604 patients followed until 1983, 62 (10.3%) had recurrences whereas the corresponding figure in the 1985 to 1988 cohort of 338 patients followed until 1993 was only 23 (6.8%).

Discussion

The current long-term study confirmed that acute PID is a most common complication of urogenital gonococcal and chlamydial infections in sexually active young women.2–4,17,30,31

The significant decrease in admissions for acute PID during the last 10 years, 1985 through 1994, was associated with the disappearance of gonococcal-associated and a large decrease of chlamydial-associated acute PID. During the same period, the recurrence rate for this disease was reduced by nearly 40%, which seemed to coincide with our measures to subject the male partners of our patients with acute PID to antibiotic treatment.25

Despite the large decrease of gonococcal acute PID in the 1970s, the total number of patients with nongonococcal acute PID increased in the middle and late 1970s (during some years, it increased by a factor of 1.7 to 1.8), and in the early 1980s, it returned to levels that corresponded with those of the early 1970s. These fluctuations were reflected by large changes in the incidence rates of acute PID per 1000 women in the 15- to 34-year-old groups, with the most pronounced changes among those 15 to 24 years of age (Fig. 2).

These fluctuations coincided with an increased use of intrauterine contraceptive devices (IUCD) in the mid-1970s,3,9,13 which later was shown to be a significant risk factor for the development of acute PID. Thus, in the middle and late 1970s, it was not unusual that these types of contraceptives often were prescribed for patients in the 15- to 34-year-old groups. Previously, we showed that only 3% and 7% of our patients used this type of contraception in 1971 and 1972, respectively, but as many as 29% used it in 19749; more than 32% of the patients 25 to 34 years old used it in the late 1970s and early 1980s.13,32 Since that time, there has been a consensus not to prescribe IUCDs to nulliparous and sexually active fertile women.33,34 Despite corrections made for the use of IUCDs as contraceptives, the total number of admissions for acute PID continued to be high in the first half of the 1980s. By inference, this might mean that the effect of IUCDs on rates of acute PID in this study was minimal. Further analysis of this factor is under way and will be reported elsewhere.

The continued high numbers of admissions for PID in the late 1970s and early 1980s might have been attributable to a high incidence of genital chlamydial infections. We know from serologic studies that serum immunoglobulin G and/or immunoglobulin M antichlamydial antibodies were demonstrated in more than 60% of our patients in the late 1970s.16 The current study also showed that genital chlamydial infections often were diagnosed and occurred in 41.3% and 32.5% of patients with acute PID who were 15 to 19 and 20 to 24 years old, respectively, during 1980 to 1984 (Table 2). Chlamydial infections were also common in other age groups. Our findings are in good agreement with those reported by other Scandinavian groups.15,16,30,35,36

Swedish research groups reported high incidences of chlamydial-associated acute PID in young women during the late 1970s.15,16,30,35 These findings led in the early and middle 1980s to liberal specimen taking, advocated by public health authorities, to diagnose and treat genital chlamydial infections. Diagnostic procedures were free of charge and were available in most areas of Sweden. These measures showed that chlamydial infections were common in young fertile women, especially in the 15- to 19-year-old group.37 Epidemiologic surveys have shown that diagnostic incidence peaks were reached in 1985 to 1987; in women, in fact, they were 20% to 25% higher than the incidence peak reached for gonorrhea in Sweden in 1970.37 Reported chlamydial infection rates have declined in women by approximately 40% to 60% for the last 7 years. The decline in our area has a pattern that is similar for all of Sweden, and it coincides with a decreasing incidence of chlamydial-associated acute PID.37,38

We are, of course, aware that the overt acute PID accounted for in this article is probably only the “tip of the iceberg” in view of the many reports on silent PID,17,38–40 whose frequency in the population can best be estimated by incidence rates for tubal factor infertility and ectopic pregnancy, or laparoscopy and endometrial biopsy in women with evidence for lower genital tract infection without signs and symptoms of acute PID.41

The current investigation shows the importance of a longitudinal study to detect variations in the epidemiology of acute PID, a clinical syndrome with several etiologies. To draw conclusions from the changes, we must ask whether these may be caused by population changes in the particular age groups studied or by changes of criteria used for admitting patients with suspected diagnoses of acute PID. We have no indication supporting the latter objection because the same diagnostic criteria were followed during the entire study period. Moreover, admissions are free of charge, which means that the majority of patients come to the emergency room because of fever and lower abdominal pain.

Because of these factors and the fact that significant changes occurred with regard to the incidence of gonorrhea and genital chlamydial infections in the catchment area and in Sweden as a whole (Fig. 3), the use of IUCDs,9,13 and recurrence rates, it was interesting to note that the different developments in incidence rates for acute PID over the time period studied were accompanied by a shift in the age distribution of patients admitted. This was most obvious for the 15- to 19-year-old and the ≥35-year-old groups. As a whole, those 15 to 29 years of age constituted approximately 80% of patients in the first 5-year period but 65% of patients in the last 5-year period. In contrast, the oldest age group represented less than 10% in the first half of the 1970s but nearly 25% of the patients 20 years later.

Fig. 3
Fig. 3:
The yearly incidences of gonorrhea and genital chlamydial infection per 100,000 population in Sweden and Örebro county. Incidence curves for gonnorrhea cover the 25-year-study period from 1970 to 1994, whereas those for genital chlamydial infection began in 1985 (voluntary reporting for this disease from Swedish laboratories was initiated in 1984).

It should be pointed out that the incidence rates were calculated in the youngest and oldest age groups (10 to 14 years and 35 to 54 years of age). These limits represent a wide age range for the disease in question. Few incidences occurred close to the lower and upper border values of 10 and 54 years, respectively. Three incidences (55, 56, 57 years old in 1991, 1972, and 1986, respectively) were above the upper limit. The calculated values of the incidence rates, therefore, may be underestimated values of a more representative incidence rate. For internal comparisons, the chosen approach was considered satisfactory. Another question concerns the definition of the catchment area of the hospital. There have been no known or anticipated changes in what was once demarcated to constitute the catchment area of the hospital.

The current 25-year-study thus showed that admissions of patients with acute PID diminished because the incidences of gonorrhea and genital chlamydial infections were reduced and recurrence was prevented. The continuous 10-year decrease can be ascribed nearly totally to women in the 15- to 34-year-old groups, which is in contrast to the continuous and relatively high proportion of acute PID in women 35 years and older. No gonorrhea or genital chlamydial infections were demonstrated in these women, who, for the last 5-year-period, were responsible for the second highest number of admissions for acute PID. The reasons to this are unclear. This patient group may represent the young cohorts from the late 1970s and early 1980s who had very high incidence rates for acute PID. It has been proposed that a previous acute episode of PID may sensitize a woman for a later attack.2–4,17 We have shown previously that 40% of the women in this age group were IUCD users,13 which might be a significant factor. At present, we are trying to elucidate these matters and will report on them elsewhere.

References

1. Centers for Disease Control. Antibiotic-resistant strains of Neisseria gonorrheae: Policy guidelines for detection, management, and control. MMWR 1987; 36(suppl 5):1–18.
2. Weström L. Incidence, prevalence, and trends of acute pelvic inflammatory disease and its consequences in industrialized countries. Am J Obstet Gynecol 1980; 138:880–892.
3. Weström L, Mårdh P-A. Acute pelvic inflammatory disease (PID). In: Holmes KK, Mårdh P-A, Sparling PF, et al, eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1990:593–613.
4. Eschenbach DA. Acute pelvic inflammatory disease. Urol Clin North Am 1984; 11:65–81.
5. Sweet RL. Pelvic inflammatory disease. Sex Transm Dis 1986; 13(suppl 3):192–198.
6. Centers for Disease Control. Chlamydia trachomatis infections: Policy guidelines for prevention. MMWR 1985; 34:53–74.
7. National Board of Health and Welfare. Chlamydia infections: Preventive strategies: General recommendations. Gotab (Stockh) 1992; 2:1–46. In Swedish.
8. Rees E, Annels EH. Gonococcal salpingitis. Br J Vener Dis 1969; 45:205–215.
9. Forslin L, Falk V, Danielsson D. Changes in the incidence of acute gonococcal and nongonococcal salpingitis: A five-year study from an urban area of central Sweden. Br J Vener Dis 1978; 54:247–250.
10. Gisslen H, Hellgren L, Starck V. Incidence, age distribution and complications of gonorrhea in Sweden: Bulletin of the World Health Organization 1961; 24:367–374.
11. Krook G, Juhlin I. Problems in diagnosis, treatment and control of gonorrheal infections: IV: The correlation between the dose of penicillin, concentration in blood, IC50 values of gonococci and results of treatment. Acta Derm Venereol (Stockh) 1965; 45:242–253. In English.
12. Lycke E, Löwhagen GB, Hallhagen G, Johannisson G, Ramstedt K. The risk of transmission of genital Chlamydia trachomatis infection is less than that of genital Neisseria gonorrhoeae infection. Sex Transm Dis 1980; 7:6–10.
13. Kamwendo F, Forslin L, Danielsson D. Epidemiology and aetiology of acute non-tuberculous salpingitis: A comparison between the early 1970s and the early 1980s with special reference to gonorrhea and use of intrauterine contraceptive device. Genitourin Med 1990; 66:324–329.
14. Mårdh P-A, Ripa T, Svensson L, Weström L. Chlamydia trachomatis infection in patients with acute salpingitis. N Engl J Med 1977; 296:1337–1379.
15. Mårdh P-A, Lind I, Svensson L, Möller BR. Antibodies to Chlamydia trachomatis, Mycoplasma hominis and Neisseria gonorhoeae in serum from patients with acute salpingitis. Br J Vener Dis 1981; 57:125–129.
16. Ripa T, Forslin L, Danielsson D, Falk V. Frequency of gonococcal and chlamydial infections in patients with laparoscopically verified acute salpingitis in 1970 and 1980: Epidemiological considerations. In: Mårdh P-A, Holmes KK, Oriel JD, Piot P, Schacter J, eds. Chlamydial Infections. Amsterdam: Elsevier Biomedical Press, 1982:179–182.
17. Cates W Jr, Rolfs RT Jr, Aral SO. Sexually transmitted diseases, pelvic inflammatory disease, and infertility: An epidemiologic update. Epidemiol Rev 1990; 12:199–220.
18. Falk V, Ludviksson K, Ågren G. Genital tuberculosis in women: Analysis of 187 newly diagnosed cases from 47 Swedish hospitals during the ten-year period 1968 to 1977. Am J Obstet Gynecol 1980; 138:974–977.
19. Punnonen R, Söderström KO, Alanen A. Isthmic tubal occlusion: Etiology and histology. Acta Eur Fertil 1984; 15:39–42.
20. Paavonen J, Teisala K, Heinonen PK, Aine R, Miettinen A, Lehtinen M, Grönroos P. Endometritis and acute salpingitis associated with Chlamydia trachomatis and Herpes simplex virus type two. Obstet Gynecol 1985; 65:288–291.
21. Familiari U, Larocca LM, Tamburrini E, Antinori A, Ortona L, Capelli A. Premenopausal cytomegalovirus oophoritis in a patient with AIDS. Abbreviated source. AIDS 1991; 5:458–459. Letter.
22. Ojwang AW, Lema VM, Wanjala SH. HIV infection among patients with acute pelvic inflammatory disease at the Kenyatta National Hospital, Nairobi, Kenya. East Afr Med J 1993; 70:506–511.
23. Irwin KL, Rice RJ, Sperling RS, O'Sullivan MJ, Brodman M. Potential for bias in studies of the influence of human immunodeficiency virus infection on the recognition, incidence, clinical course, and microbiology of pelvic inflammatory disease. Obstet Gynecol 1994; 84:463–469.
24. Control of Infectious Diseases Act. SFS (Swedish code of law) 1968:231; 1988:1472.
25. Kamwendo F, Johansson E, Moi H, Forslin L, Danielsson D. Gonorrhea, genital chlamydial infection, and nonspecific urethritis in male partners of women hospitalized and treated for acute pelvic inflammatory disease. Sex Transm Dis 1993; 20:143–146.
26. Holmes KK. Lower genital tract infections: Cystitis, urethritis, vulvovaginitis, and cervicitis. In: Holmes KK, Mårdh P-A, Sparling PF, et al, eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1990:527–545.
27. Jacobson L, Weström L. Objectivized diagnosis of acute pelvic inflammatory disease. Am J Obstet Gynecol 1969; 105:1088–1098.
28. Mårdh P-A, Danielsson D. Neisseria gonorrhoeae. In: Holmes KK, Mårdh P-A, Sparling PF, et al, eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1990:903–916.
29. Stamm WE, Mårdh P-A. Chlamydia trachomatis. In: Holmes KK, Mårdh P-A, Sparling PF, et al, eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1990:917–925.
30. Osser S, Persson K. Epidemiologic and serodiagnostic aspects of chlamydial salpingitis. Obstet Gynecol 1982; 59:206–209.
31. Brihmer C, Kallings I, Nord C-E, Brundin J. Salpingitis: Aspects of diagnosis and etiology: A 4-year study from a Swedish capital hospital. Eur J Obstet Gynecol Reprod Biol 1987; 24:11–20.
32. National Central Bureau of Statistics. Women and children—interviews with women about family and work: Forecasting information. 1982; 4:33–41.
33. Nygren K-G, Odlind V. Anticonception. In: The National Cooperation of Swedish Pharmacists: Book of Therapeutic Drugs (Läkemedelsboken). Uppsala, Sweden: Almquist & Wiksell AB, 1985:976–989.
34. The National Board of Health and Welfare. General advice from the National Board of Health and Welfare: Contraceptives—current pregnancy preventive methods. Stockholm: Modin-Tryck AB, 1987:1–54.
35. Ripa KT, Svensson L, Treharne JD, Weström L, Mårdh P-A. Chlamydia trachomatis infection in patients with laparoscopically verified acute salpingitis: Results of isolation and antibody determinations. Am J Obstet Gynecol 1980; 138:960–964.
36. Paavonen J. Chlamydia trachomatis in acute salpingitis. Am J Obstet Gynecol 1980; 138:957–959.
37. Kihlström E, Danielsson D. Advances in biology, management and prevention of infections caused by Chlamydia trachomatis and Neisseria gonorrhoeae. Curr Opin Infect Dis 1994; 7:25–33.
38. Weström L. Decrease in incidences of women treated in hospital for acute salpingitis in Sweden. Genitourin Med 1988; 64:59–63.
39. Wölner-Hanssen P, Kiviat NB, Holmes KK. Atypical pelvic inflammatory disease: Subacute, chronic, or subclinical upper genital tract infection in women. In: Holmes KK, Mårdh P-A, Sparling PF, et al, eds. Sexually Transmitted Diseases. New York: McGraw-Hill; 1990:615–620.
40. Berger GS, Weström LV, Wölner-Hanssen P. Definition of pelvic inflammatory disease. In: Berger GS, Weström LV, eds. Pelvic Inflammatory Disease. New York: Raven Press, 1992:1–6.
41. Padian NS, Washington AE. Pelvic inflammatory disease: A brief overview. Ann Epidemiol 1994; 4:128–132.

Epidemiology and Prevention of Infectious Diseases; February 6–8, 1997; Fairmount Hotel atop Nob Hill; San Francisco, California

This program provides an overview of the scope and methods used in infectious disease epidemiology and research, the unique aspects of hospital epidemiology and infection control, and the epidemiology and prevention of specific infectious diseases. The program is designed for all practitioners in the disciplines of epidemiology, public health, health administration, medicine, nursing, and related professions.

The format features lectures and discussion with faculty. Topics to be covered include:

  • HIV infection
  • Tuberculosis
  • Sexually transmitted diseases
  • Meningitis
  • Lyme disease
  • Haemophilus influenzae infection

Chaired by John E. Conte, Jr., MD, this program is presented by the Department of Epidemiology and Biostatistics of the University of California School of Medicine at San Francisco. The program is sponsored by the UCSF's Office of Continuing Medical Education.

UCSF is accredited by the Accreditation Council for Continuing Medical Education. This program will meet the criteria for category 1 credit.

For further information, please write or call the Office of Continuing Medical Education, Room MCB-630, University of California, San Francisco, CA 94143-0742, (415) 476–4251

© Copyright 1996 American Sexually Transmitted Diseases Association